Expresión y Modulación del Receptor de Prolactina en Células Inmunes: Inducción de ARNm y Proteínas por Dexametasona

SANCHEZ, BELÉN; JUAN PABLO MACKERN OVERTI; RIVERO, VIRGINIA ELENA; MARÍA TAMARA MORENO SOSA; GRACIELA ALMA JAHN

San Luis

Congreso; XXXVII Reunión Científica Anual de la SBCuyo; 2019

Sociedad de Biología de Cuyo

Prolactin (PRL) is a peptide hormone that performs functions in modulating the immune response. PRL actions are mediated by its receptor isoforms (PRL-R) that differ in their intracellular portion and therefore in the signaling pathway they trigger. It is known that there is a relationship between PRL and different autoimmune pathologies, such as systemic lupus erythematosus and rheumatoid arthritis, so it is of interest to clarify its real participation in the immune system. The aim of this work is to analyze the expression of PRL-R isoforms in human and murine immune system cells, and determine if there is there are modulated in the regulation of the immune response after stimulation with Concanavalin A and Dexamethasone. For this end, cells of the immune system were extracted from the spleen of female mice and human peripheral blood. For the induction tests of the immune system, murine splenocytes were stimulated with 1 µg/ml of Concanavalin A or Dexamethasone and kept in culture for 24 hours. The samples were purified for subsequent RNA extraction and cDNA synthesis. Protein determination was carried out by flow cytometry, where murine splenocytes were labeled with Anti-CD4, Anti-CD19 and Anti-PRL-R antibodies conjugated with fluorochromes. It was found that both human and murine immune system cells express the long and short isoforms of PRL-R. In addition, it was observed that PRL-R expression is not altered after stimulation with concanavalin A, however, it increases after stimulation with dexamethasone. Although more studies are required, these data provide evidence of participation of PRL-R isoforms in the mechanisms of immuno-endocrine regulation directed by PRL.